ERRATAS AND CLARIFICATION

Page 41
Under 1. Acute inflammation (see Fig. 2-13A)
Under 2. Chronic inflammation (see Figure 2-13B)

Page 106
Margin note
Triple marker for Down syndrome: decreased AFP, increased hCG, decreased urine
estriol

Page 128
Under D. Vitamin K, 3. Function
a. γ-Carboxylates glutamate residues in vitamin K-dependent procoagulants and
anticoagulants (protein C and S)
(1) Procoagulants include factors II (prothrombin), VII, IX, and X (delete protein C and
S, which are anticoagulants)

Page 129
Table 7-3
Thiamine (vitamin B1)
Korsakoff’s psychosis: antegrade and retrograde

Page 138
D. Growth rate
3. Thirty doubling…
• Equivalent to 109…..

Page 142
Table 8-1
Autosomal dominant cancer syndromes
(two-hit theory)

Page 145
5. DNA repair genes (see Table 8-1 and Table 8-4)

Page 154
4. Apolipoprotein B deficiency (abetalipoproteinemia)
a. Autosomal recessive

Page 162
Table 9-1
Under Sturge-Weber syndrome
Delete (AD)
Actually, it is now considered somatic mosacism
Page 173
Under Prinzmetal’s angina
increase in endothelin

Page 182
Tetralogy of Fallot
(7) Tet spells
(a) Sudden increase in hypoxemia and cyanosis

Page 203
Under C. 3. (c) Microcytic and normocytic cells with increased central area of pallor
(Fig. 11-6)

Page 300
Put Chlamydia, Rickettsia, Mycoplasma under Bacteria not Viruses heading

Page 323
Table 16-5
Under Bronchial hamartoma
Put− Peripheral (90%), Central (10%)

Page 352
Table 17-7
Under Hernia
Direct
Medial border of triangle is rectus abdominis muscle, lateral border is inferior epigastric
artery, inferior border is inguinal ligament

Page 358
c. Peutz-Jeghers polyposis
(1) Autosomal dominant
(2) Polyps predominate in the small bowel; less common in stomach and colon
MN: Peutz-Jeghers polyposis: predominance of small intestine polyps
In Anderson’s textbook of Pathology and Sabiston’s Surgery, Peutz-Jeghers polyps are
listed as hamartomas, because they are a non-neoplastic overgrowth of normal tissue. In
all the major texts, the small intestine is listed as the most common site for the polyps.
They are less common in stomach and colon. Key point is that it is the only hereditary
polyposis syndrome with polyps more common in the small intestine than the colon.

Juvenile polyps are listed as hamartomatous polyps in Anderson’s Pathology and Morson
Gastrointestinal Pathology. They are sometimes called retention polyps.

Hyperplastic polyps are non-neoplastic polyps that some purists consider hamartomas
and others a type of metaplasia, with mucosa resembling small bowel. The key point is
that they are non-neoplastic and do not transform into cancer.
Page 371
Under e. Chronic HBV, (1) …converts to anti-HBc-IgG

Page 375
Margin Note
Fulminant hepatic failure: ↓ transaminases, ↑ PT and ammonia

Pages 377 and 378

Under A. Alcohol related disorders
1. should say (Chapter 6)
3. should say (Chapter 6)
4. should say (Chapter 6)

Page 396
Table 19-1
Glomerular Nephritic syndrome: Damage of GBM: non-selective proteinuria with
protein > 150 mg/ loss of albumin and globulins; example is post-
24 hours but streptococcal glomerulonephritis
< 3.5 g/24 hours
Nephrotic syndrome: Loss of negative charge on GBM: selective
protein > 3.5 g/24 proteinuria with loss of albumin and not
hours globulins; example is minimal change disease

I moved the causes of glomerular proteinuria to line-up with nephritic and nephrotic.
The original table was not intended to match up the cause of glomerular proteinuria with
an example of a nephritic syndrome and nephrotic syndrome. Because this has caused
confusion, I changed diffuse membranous glomerulopathy, the most common cause of
nephrotic syndrome in adults, to post-streptococcal glomerulonephritis and lined this up
with nephritic syndrome and minimal change disease, the most common cause of
nephrotic syndrome in children, with nephrotic syndrome. In the original table, it looked
like I was implying that minimal change disease was an example of glomerular injury in
the nephritic syndrome, which is of course, incorrect.

Page 395
B. Serum creatinine
2. Creatinine is filtered in the kidneys and not reabsorbed or secreted
This sentence is a generality and is true at the normal concentration of creatinine. It was
not part of a discussion of renal failure or of variations of creatinine in emaciated
individuals versus muscular people or the effect of drugs on the measurement of serum
creatinine. It is true that at high serum levels of creatinine, some is secreted into the urine,
so it overestimates the creatinine clearance in renal failure; however, many other tests
help corroborate the severity of the renal failure like serum calcium, phosphorus, BUN,
and electrolytes showing hyperkalemia and metabolic acidosis. However, irrespective of
this, the creatinine clearance is a more practical and cost effective test even though it is
not a perfect clearance substance like inulin.
Page 409
Table 19-7
Change IgA glomerulonephritis to IgA glomerulopathy
Page 412
Table 19-8
Type I MPGN
Subendothelial ICs

Page 443
3. Prolactin
a. Prolactin enhances testosterone function and spermatogenesis.
A number of articles discuss the important role that prolactin normally has in promoting
the function of the testis and accessory structures. Prolactin receptors are present in the
Leydig cells, differentiating germ cells in the seminiferous tubules, and all of the
accessory structures. Specifically, in the Leydig cells, prolactin is important in inducing
and maintaining LH receptors; which enhances testosterone function. It also directly has
an effect on enhancing spermatogenesis. When prolactin is increased, it shuts off GnRH;
which, in turn, decreases testosterone production (LH effect) and spermatogenesis (FSH)
effect.

Page 446 (not an errata; just a better term

IX. Erectile dysfunction
Drop the definition underneath since it is self-explanatory

Page 479
Under 3. Traumatic fat necrosis
c. Painless, indurated mass
add: • Painful in acute stage

Page 504 Table 22-3

Pseudohypoparathyroidism: autosomal dominant

Page 505 Clarification

Hypertension in hypercalcemia:
Hypertension is seen with increased frequency in patients with hypercalcemia (e.g.,
primary hyperparathyroidism). It may be caused by renal insufficiency and/or calcium-
mediated vasoconstriction of arterioles.

Page 516 (not an errata; just an additional designation)

C. Syndrome X (metabolic syndrome)

Page 532
Under Septic arthritis, change C5-C9 to C6-C9.
Page 537
Table 23-3
Compartment syndrome
Volkmann’s ischemic contracture: supracondylar fracture of humerus….

Page 543
Under A. Staphylococcus aureus skin infections
Add d. Impetigo

Page 544
Under C. Impetigo
1. Most often caused by Staphylococcus aureus
• Streptococcus pyogenes second most common cause
3. Presence of bullae commonly occurs with Staphylococcus aureus

Page 551-552
2. Pemphigus vulgaris (page 551)
c. Intraepithelial vesicles are located above the basal layer (suprabasal).
(3) Positive Nikolsky sign
• Outer epidermis separates from basal layer with minimal pressure
3. Bullous pemphigoid (page 552)
b. Vesicles are subepidermal.
(3) Negative Nikolsky sign

The oral mucosa is involved in one-third of cases, which is not rare as one medical
student suggested on an Internet site. This was a really bad mistake in editing, because I
had in correct in the notes I used to teach students with before the book came out.

Page 569
Under 4. Sturge-Weber syndrome
a. Somatic mosaicism or sporadic
It is not autosomal dominant

Page 578, Table 25-2

Under Rabies virus: Most often transmitted by raccoon bite (40%)

Other vectors are dog, skunk, bat, coyote

Page 579
Under Table 25-4: Treponema pallidum
Argyll-Robertson pupil (pupils accommodate but do not react)
Page 583
2. Role of beta-amyloid (Abeta) protein
b. Defects in degradation of APP by secretases cause an increase in Abeta
(1) Alpha-secretases cleave APP into fragments that cannot produce Abeta
(2) Beta and gamma-secretases cleave APP into fragments that are converted to
Abeta.
Beta secretases first must cleave (“clip”) the APP and then subsequent cleavage by
gamma secretases produces Abeta, which forms amyloid that is neurotoxic.

Page 585
Figure 25-17
Coronal section (B) shows (leave out dilated lateral ventricle and) atrophy of the caudate,
putamen, and globus pallidus when compared with a normal coronal section (A).
A different picture was placed in there during publication, but the original discussion was
not changed. The above is a correct discussion of the new picture.

Page 586
Under F. Werdnig-Hoffman disease
• Lower motor neuron disease that occurs in children.

QUESTION 10 (Page 652 has question, page 657 has discussion)

A 9-month-old girl has an infection on her face that began as erythematous macules. She
later develops pustules that rupture and cause honey-colored crusted lesions. The girl's 5-
year-old brother develops similar lesions. Which of the following is the causal agent?

A. Staphylococcus aureus
B. Herpes simplex virus type 1
C. Malassezia furfur
D. Propionibacterium acnes
E. Trichophyton rubrum

A (Staphylococcus aureus) is correct. The child has impetigo, which causes honey-
colored crusted lesions that cover shallow ulcerations of the skin. Staphylococcus aureus
is the most common cause of this superficial skin lesion. Streptococcus pyogenes is the
second most common cause of impetigo. Impetigo is highly contagious, which explains
why the child's brother develops similar lesions.

B (herpes simplex virus type 1) is incorrect. Herpes simplex virus type 1 produces
vesicles and pustules on the vermilion border of the lip. It does not produce honey-
colored crusted lesions on the face.
C (Malassezia furfur) is incorrect. M. furfur, a superficial dermatophyte, causes tinea
versicolor and seborrheic dermatitis (dandruff). It does not produce honey-colored
crusted lesions on the face.
D (Propionibacterium acnes) is incorrect. P. acnes is an anaerobe involved in producing
the inflammatory reaction associated with acne vulgaris. It does not produce honey-
colored crusted lesions on the face.
E (Trichophyton rubrum) is incorrect. T. rubrum, a superficial dermatophyte, causes tinea
corporis (body), tinea cruris (groin), and tinea pedis (foot). It does not produce honey-
colored crusted lesions on the face.